Evidence map›Paper›PMID 41205188›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Bifurcate Regulation of Hematopoietic Homeostasis and Bone Osteogenesis by VHL-HIF2α-Controlled Adipocyte Function.

Qian Li, Jia Li, Anshu Tang, Cong Li, Chao Zhang, Congcong Zhang, Yun-Cai Liu

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Qian LiInstitute for Immunology and School of Basic Medical Sciences, Tsinghua University, Beijing, 100084, China.ORCID https://orcid.org/0009-0001-6907-2833
Jia LiInstitute for Immunology and School of Basic Medical Sciences, Tsinghua University, Beijing, 100084, China.
Anshu TangInstitute for Immunology and School of Basic Medical Sciences, Tsinghua University, Beijing, 100084, China.
Cong LiInstitute for Immunology and School of Basic Medical Sciences, Tsinghua University, Beijing, 100084, China.
Chao ZhangInstitute for Immunology and School of Basic Medical Sciences, Tsinghua University, Beijing, 100084, China.
Congcong ZhangInstitute for Immunology and School of Basic Medical Sciences, Tsinghua University, Beijing, 100084, China.
Yun-Cai LiuInstitute for Immunology and School of Basic Medical Sciences, Tsinghua University, Beijing, 100084, China.

Funding

Ministry of Science and Technology of the People's Republic of China 2021YFC2300503National Natural Science Foundation of China 81871225National Natural Science Foundation of China 82130051Tsinghua University-Xiamen Chang Gung Hospital Joint Research Center for Anaphylactic Disease
6 · The paper itself

Abstract

Adipocytes play a pivotal role in maintaining metabolic and immunological homeostasis. Here, this work shows that VHL-HIF2α (VHL is Von Hippel-Lindau) axis in mature adipocytes regulates hematopoiesis and osteogenesis. Genetic ablation of VHL in adipocytes triggers profound systemic autoinflammation and abnormal hematopoiesis, concomitant with fat mass decrease and pathological elevation of bone mass. On one hand, VHL deficiency results in aberrantly high stem cell factor (SCF) expression in adipocytes, which exerts a negative role for hematopoietic homeostasis through disrupting hematopoietic stem cell (HSC) quiescence. In vivo anti-CD117 monoclonal antibody treatment ameliorates the hematopoietic defects in VHL-deficient mice. On the other hand, direct HIF2α binding to hypoxia-response elements in the Rarres2 locus enhances chemerin production in adipocytes, which facilitates mesenchymal stem cell (MSC) osteogenesis via Wnt/β-catenin activation. Pharmacological chemerin neutralization through CMKLR1 inhibition using α-NETA mitigates osteogenic activity both in vitro and in vivo. This work thus identifies chemerin as the pivotal molecular nexus connecting hypoxic adipocyte dysfunction to pathological osteosclerosis. The findings uncover a hypoxia-driven signaling network in adipocytes that orchestrates cross-talk with both HSCs and MSCs to regulate systemic homeostasis, thereby revealing therapeutic targets for disorders associated with adipocyte dysfunction.

Indexed as

AdipocytesBasic Helix-Loop-Helix ProteinsHematopoiesisHomeostasisOsteogenesisVon Hippel-Lindau Tumor Suppressor ProteinAnimalsChemokinesHematopoietic Stem CellsIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, KnockoutBasic Helix-Loop-Helix Proteinschemerin protein, mouseChemokinesIntercellular Signaling Peptides and ProteinsVHL protein, mouseVon Hippel-Lindau Tumor Suppressor ProteinadipogenesishematopoiesisosteosclerosisVHL‐HIF axis

Identifiers

PMID41205188
PMCPMC12850111

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.